Dataset Information

Performance of urine cotinine and hypomethylation of AHRR and F2RL3 as biomarkers for smoking exposure in a population-based cohort.

ABSTRACT: There is a growing body of evidence demonstrating an association between smoking and DNA methylation. Accordingly, DNA methylation is now considered a promising biomarker of smoking exposure. We evaluated the relationship between methylation markers (AHRR and F2RL3) and urine cotinine as well as self-reported smoking status. DNA methylation levels of AHRR and F2RL3 in blood as well as urine cotinine were measured in 330 adults (46 to 87 years of age). Pyrosequencing was performed to measure DNA methylation of AHRR and F2RL3 associated with smoking exposure. The lung cancer risk associated with DNA methylation and urine cotinine was analyzed using logistic regression analysis. The AHRR and F2RL3 genes were significantly hypomethylated in current smokers compared to in individuals who have never smoked. An inverse relationship was observed between urine cotinine and methylation levels. Methylation of AHRR and F2RL3 distinguished current smokers from never-smokers with high accuracy. Logistic multivariate analysis showed that AHRR methylation is significantly associated with the risk of lung cancer (OR = 0.96, P = 0.011). Our study validated the smoking-associated DNA methylation markers reported in a Korean population-based cohort. In conclusion, DNA methylation of AHRR and F2RL3 provided accurate measures for smoking exposure. Methylation markers reflecting the long-term effect of smoking on the risk of lung cancer showed better performance in distinguishing former smokers from never-smokers.

SUBMITTER: Lee DH

PROVIDER: S-EPMC5409156 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Performance of urine cotinine and hypomethylation of AHRR and F2RL3 as biomarkers for smoking exposure in a population-based cohort.

Lee Do-Hoon DH Hwang Sang-Hyun SH Lim Min Kyung MK Oh Jin-Kyoung JK Song Da Young DY Yun E Hwa EH Park Eun Young EY

PloS one 20170428 4

There is a growing body of evidence demonstrating an association between smoking and DNA methylation. Accordingly, DNA methylation is now considered a promising biomarker of smoking exposure. We evaluated the relationship between methylation markers (AHRR and F2RL3) and urine cotinine as well as self-reported smoking status. DNA methylation levels of AHRR and F2RL3 in blood as well as urine cotinine were measured in 330 adults (46 to 87 years of age). Pyrosequencing was performed to measure DNA ...[more]

PMID: 28453567

Similar Datasets

Project description:BackgroundWelders are at risk for cardiovascular disease. Recent studies linked tobacco smoke exposure to hypomethylation of the F2RL3 (coagulation factor II (thrombin) receptor-like 3) gene, a marker for cardiovascular disease prognosis and mortality. However, whether welding fumes cause hypomethylation of F2RL3 remains unknown.MethodsWe investigated 101 welders (median span of working as a welder: 7 years) and 127 unexposed controls (non-welders with no obvious exposure to respirable dust at work), age range 23-60 years, all currently non-smoking, in Sweden. The participants were interviewed about their work history, lifestyle factors and diseases. Personal sampling of respirable dust was performed for the welders. DNA methylation of F2RL3 in blood was assessed by pyrosequencing of four CpG sites, CpG_2 (corresponds to cg03636183) to CpG_5, in F2RL3. Multivariable linear regression analysis was used to assess the association between exposure to welding fumes and F2RL3 methylation.ResultsWelders had 2.6% lower methylation of CpG_5 than controls (p<0.001). Higher concentrations of measured respirable dust among the welders were associated with hypomethylation of CpG_2, CpG_4 and CpG_5 (β=-0.49 to -1.4, p<0.012); p<0.029 adjusted for age, previous smoking, passive smoking, education, current residence and respirator use. Increasing the number of years working as a welder was associated with hypomethylation of CpG_4 (linear regression analysis, β=-0.11, p=0.039, adjusted for previous smoking). Previous tobacco smokers had 1.5-4.7% (p<0.014) lower methylation of 3 of the 4 CpG sites in F2RL3 (CpG_2, CpG_4 and CpG_5) compared to never-smokers. A non-significant lower risk of cardiovascular disease with more methylation was observed for all CpG sites.ConclusionsWelding fumes exposure and previous smoking were associated with F2RL3 hypomethylation. This finding links low-to-moderate exposure to welding fumes to adverse effects on the cardiovascular system, and suggests a potential mechanistic pathway for this link, via epigenetic effects on F2RL3 expression.

Project description:ObjectivesCotinine is the gold standard to estimate prevalence of secondhand tobacco smoke (SHS) exposure, and assay limit of detection (LOD) cut-points are typically used regardless of age. Our aim was to compare the concordance between mother-reported SHS exposure and serum cotinine categorising children as exposed with the assay LOD or age-specific cut-points.DesignData from the Health Outcomes and Measures of the Environment (HOME) Study, a prospective pregnancy and birth cohort.SettingHospital or participants' homes.Participants389 pregnant women aged 18 years and older, between 13 and 19 weeks of gestation, living in a five-county region of the Cincinnati, Ohio metropolitan area, and with follow-up on their children at birth and ages 12, 24, 36 and 48 months.Primary and secondary outcome measuresChildren's serum cotinine, mother-reported active smoking and SHS exposure were available at birth and during follow-up visits. We used Cohen's kappa index to assess concordance between maternal self-report and child's serum cotinine concentrations. We estimated optimal age-specific cut-points, their sensitivity-specificity and positive-negative predictive values with receiver operating characteristic curves.ResultsSelf-reported exposure and cotinine data were available for 280 women who gave birth to singleton child. When applying the assay LOD (0.015 ng/mL), concordance between maternal report and serum cotinine, without accounting for age, was below 0.23 at all times. When using age-specific cut-points (12 months: 0.11 ng/mL; 24 months: 0.08 ng/mL; 36 months: 0.05 ng/mL and 48 months: 0.04 ng/mL), concordance improved, being low at 12 months (0.39), moderate at 24 and 36 months (0.47 and 0.43) and high at 48 months (0.62).ConclusionsConcordance between mother-reported SHS exposure among children under 5 years and serum cotinine improved considerably after applying the cohort-specific and age-specific cut-points. Future studies are necessary to verify these results.

Project description:BackgroundChildren may be exposed to tobacco products in multiple ways if their parents smoke. The risks of exposure to secondhand smoke (SHS) are well known. This study aimed to investigate the association between parental smoking and the children's cotinine level in relation to restricting home smoking, in Korea.MethodsUsing the Korea National Health and Nutrition Health Examination Survey data from 2014 to 2017, we analyzed urine cotinine data of parents and their non-smoking children (n = 1,403), in whose homes parents prohibited smoking. We performed linear regression analysis by adjusting age, sex, house type, and household income to determine if parent smoking was related to the urine cotinine concentration of their children. In addition, analysis of covariance and Tukey's post-hoc tests were performed according to parent smoking pattern.FindingChildren's urine cotinine concentrations were positively associated with those of their parents. Children of smoking parents had a significantly higher urine cotinine concentration than that in the group where both parents are non-smokers (diff = 0.933, P < .0001); mothers-only smoker group (diff = 0.511, P = 0.042); and fathers-only smoker group (diff = 0.712, P < .0001). In the fathers-only smoker group, the urine cotinine concentration was significantly higher than that in the group where both parents were non-smoker (diff = 0.221, P < .0001), but not significantly different compared to the mothers-only smoker group (diff = - -0.201, P = 0.388). Children living in apartments were more likely to be exposed to smoking substances.ConclusionThis study showed a correlation between parents' and children's urine cotinine concentrations, supporting the occurrence of home smoking exposure due to the parents' smoking habit in Korea. Although avoiding indoor home smoking can decrease the children's exposure to tobacco, there is a need to identify other ways of smoking exposure and ensure appropriate monitoring and enforcement of banning smoking in the home.

Dataset Information

Performance of urine cotinine and hypomethylation of AHRR and F2RL3 as biomarkers for smoking exposure in a population-based cohort.

Publications

Performance of urine cotinine and hypomethylation of AHRR and F2RL3 as biomarkers for smoking exposure in a population-based cohort.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets